During fiscal year 2010 we accomplished the following: 1) We used Bim-deficient and Fas-deficient CD4+ T cells to dissect the contributions of mitochondrial and death receptor-initiated pathways of activation-induced cell death. We found that the COX2 inhibitor celecoxib increased mitochondria-dependent cell death without significantly affecting death-receptor initiated cell death. These observation were confirmed in CD4+ T cells from COX2-deficient mice. Gene expression changes in the presence of celecoxib were evaluated by microarray analysis of cells activated for different time periods in the presence or absence of the drug. 2) We found that earlier studies of Dicer-deficient cells were compromised by outgrowth of Dicer-sufficient cells during preparation of T cell blasts. These studies are currently being repeated with cells that express transgenic BclXL to prevent cell death during the first activation phase. 3) We used quantitative reverse-transcriptase PCR to identify changes in micro-RNA expression in cells activated for different time periods. These results will be evaluated in the context of responses of Dicer-deficient CD4+ T cells to identify the role of micro RNAs in regulating cell death.